N-Acetylcysteine Supplementation Controls Total Antioxidant Capacity, Creatine Kinase, Lactate, and Tumor Necrotic Factor-Alpha against Oxidative Stress Induced by Graded Exercise in Sedentary Men
Author(s) -
Donrawee Leelarungrayub,
Raphiphat Khansuwan,
Prapas Pothongsunun,
Jakkrit Klaphajone
Publication year - 2011
Publication title -
oxidative medicine and cellular longevity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.494
H-Index - 93
eISSN - 1942-0900
pISSN - 1942-0994
DOI - 10.1155/2011/329643
Subject(s) - creatine kinase , medicine , oxidative stress , endocrinology , acetylcysteine , antioxidant , vo2 max , treadmill , tumor necrosis factor alpha , creatine , chemistry , biochemistry , heart rate , blood pressure
Aim of this study was to evaluate the effects of short-term (7 days) N-acetylcysteine (NAC) at 1,200 mg daily supplementation on muscle fatigue, maximal oxygen uptake (VO 2max ), total antioxidant capacity (TAC), lactate, creatine kinase (CK), and tumor necrotic factor-alpha (TNF- α ). Twenty-nine sedentary men (13 controls; 16 in the supplement group) from a randomized control were included. At before and after supplementation, fatigue index (FI) was evaluated in the quadriceps muscle, and performed a graded exercise treadmill test to induce oxidative stress, and as a measure of VO 2max . Blood samples were taken before exercise and 20 minutes after it at before and after supplementation, to determine TAC, CK, lactate, and TNF- α levels. Results showed that FI and VO 2max increased significantly in the supplement group. After exercise decreased the levels of TAC and increased lactate, CK, and TNF- α of both groups at before supplementation. After supplementation, lactate, CK, and TNF- α levels significantly increased and TAC decreased after exercise in the control group. Whereas the TAC and lactate levels did not change significantly, but CK and TNF- α increased significantly in the supplement group. Therefore, this results showed that NAC improved the muscle fatigue, VO 2max , maintained TAC, controlled lactate production, but had no influence on CK and TNF- α .
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